http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : ( Kyuhyung Jo ) (검색결과 20 건)
- 무료
- 기관 내 무료
- 유료
-
Aster koraiensis extract improves impaired skin wound healing during hyperglycemia
현수왕,김정현,Kyuhyung Jo,Jin Sook Kim,김찬식 한국한의학연구원 2018 Integrative Medicine Research Vol.7 No.4
Background: Diabetes mellitus (DM) is one of the most common diseases found across the world. Aster koraiensis extract (AKE) has a protective effect on diabetic complications such as diabetic retinopathy. However, the effects of AKE on hyperglycemia-linked impairment of wound healing during DM have not been elucidated. In this study, we investigated the effects of AKE on delayed wound healing induced by DM. Methods: DM was induced by intraperitoneal administration of streptozotocin (STZ; 75 mg/kg) to Sprague Dawley (SD) rats. Next, a wound was induced on the back of rats after administration of STZ. Further, AKE was prepared using an alcoholic extraction of A. koraiensis and orally administered daily for 18 days. Wound healing was evaluated using an in vitro migration assay and measuring the wound area in vivo. Skin tissue thickness was evaluated using hematoxylin and eosin staining. Matrix metalloprotease (MMP) activity and expression were detected using zymography and immunohistochemistry. Results: AKE administration improved the delayed migration of keratinocytes in hyperglycemic animals. It also attenuated an increase in keratinocyte MMP-2/9 activity induced by hyperglycemia. AKE protected against DM-induced impaired wound healing in rats and prevented the degradation of skin tissue induced by DM. In addition, AKE attenuated DM-induced increase in MMP-2/9 expression in skin tissue. Conclusions: In conclusion, AKE may promote wound healing by re-epithelization via promotion of keratinocyte migration and by attenuating the disruption of the skin tissue layer via MMP-2/9 inhibition during hyperglycemia.
-
( Bongkyun Park ),( Kyuhyung Jo ),( Tae Gu Lee ),( Ik Soo Lee ),( Jin Sook Kim ),( Chan-sik Kim ) 한국운동영양학회 2019 Physical Activity and Nutrition (Phys Act Nutr) Vol.23 No.4
[Purpose] Here, we aimed to determine the effect of Polygonum cuspidatum stem extract (PSE) on exorbital lacrimal gland-excised rat models and hyperosmotic stress-stimulated human conjunctival cells (HCCs). [Methods] Seven week old male Wistar rats were divided into six groups. Only the rats in the control group (NOR, n=5) did not undergo surgery. Three days after the surgery, the exorbital lacrimal gland-excised rats were randomly allocated to five groups: (1) vehicle- treated dry-eyed rats (DED, n=5); (2) PSE (10 mg/ kg) treated DED rats (PSE-10, n=5); (3) PSE (100 mg/ kg) treated DED rats (PSE-100, n=5); and (4) PSE (250 mg/kg) treated DED rats (PSE-250, n=5). In addition, the HCC line was co-treated with hyperosmolar media (528 mOsm) and PSE (1-100 μg/ml). [Results] PSE treatment restored the tear volume and goblet cell density by inhibiting severe corneal irregularities and damage. The treatment with PSE significantly attenuated the hyperosmolar stress-induced inflammation and cell death through the suppression of mRNA expression levels of Tumor necrosis factor-α (TNF-α), Interleukin-6 (IL-6), Interleukin-1β (IL-1β), and Interferon- γ (IFN-γ), and the expression of Bcl-2-associated X protein (Bax) as well as the activation of caspase-3 in vitro. [Conclusion] The inhibitory effects of PSE treatment on dry eye disease indicate the potential of nutritional intervention by PES against inflammatory diseases without adverse effects.
-
-
( Chan-sik Kim ),( Kyuhyung Jo ),( Mi-kyung Pyo ),( Jin Sook Kim ),( Junghyun Kim ) 한국운동영양학회 2017 Physical Activity and Nutrition (Phys Act Nutr) Vol.21 No.2
[Purpose] GS-E3D is a newly developed pectin lyase-modified red ginseng extract. The purpose of this study was to evaluate the inhibitory effects of GS-E3D against ad-vanced glycation end products. [Methods] In this study, we evaluated the in-hibitory effects of GS-E3D on the formation of advanced glycation end products (AGEs) and their cross-linking with collagen in vitro and in streptozotocin-induced diabetic rats. [Results] An in vitro assay for the glycation of bovine serum albumin by methylglyoxal showed that GS-E3D inhibited AGE formation at an IC<sub>50</sub> value of 19.65 ± 4.35 μg/mL. In addition, GS-E3D showed a potent inhibitory effect (IC<sub>50</sub> = 0.42 ± 0.08 mg/mL) on the cross-linking of AGEs with collagen. However, GS-E3D showed no effect on preformed AGEs cross-linked with collagen in the breakdown assay. To determine whether GS-E3D inhibits AGE formation and their cross-linking with proteins in vivo, streptozotocin induced diabetic rats were treated with GS-E3D (25, 50, and 100 mg/kg/day) for 6 weeks. The administration of GS-E3D decreased serum levels of AGEs and their cross linking with proteins in diabetic rats. [Conclusion] The inhibitory effects of this agent on advanced glycation in vitro and in vivo suggested that it may have a potential therapeutic role in controlling diabetes-in-duced AGE burden in various tissues.
-
-
KIM, CHAN-SIK,KIM, JUNGHYUN,JO, KYUHYUNG,LEE, YUN MI,SOHN, EUNJIN,YOO, NAM HEE,KIM, JIN SOOK SPANDIDOS PUBLICATIONS 2015 MOLECULAR MEDICINE REPORTS Vol.12 No.5
<P>In the pathophysiology of diabetic retinopathy (DR), advanced glycation end products (AGEs) and vascular endothelial growth factor (VEGF) are thought to have important roles. It is known that VEGF causes a breakdown of the blood-retinal barrier (BRB) and retinal neovascularization; however, how AGEs affect the retina has largely remained elusive. OSSC1E-K19 is a novel phytochemical component of <I>Osteomeles schwerinae</I>. The objective of the present study was to evaluate the protective effects of OSSC1E-K19 on retinal vascular injury in AGE-modified rat serum albumin (AGE-RSA)-induced retinopathy. AGE-RSA-injected rat eyes were used investigate the protective effects of OSSC1E-K19 on BRB breakdown. Intravitreal injection of OSSC1E-K19 prevented AGE-RSA-induced BRB breakdown and decreased retinal VEGF expression in retinal vessels. In addition, OSSC1E-K19 inhibited the loss of occludin, a significant tight junction protein. These results supported the potential therapeutic utility of OSSC1E-K19 for retinal vascular permeability diseases.</P>
-
김정현,Ohn Soon Kim,김찬식,Eunjin Sohn,Kyuhyung Jo,JinSookKim 생화학분자생물학회 2012 Experimental and molecular medicine Vol.44 No.2
The formation of advanced glycation end products (AGEs) has been considered to be a potential causative factor of injury to lens epithelial cells (LECs). Damage of LECs is believed to contribute to cataract formation. The purpose of this study was to investigate the cytotoxic effect of AGEs on LECs both in vitro and in vivo. We examined the accumulation of argpyrimidine, a methylglyoxal-derived AGE, and the expression of apoptosis-related molecules including nuclear factor-kappaB (NF-κB), Bax, and Bcl-2 in the human LEC line HLE-B3 and in cataractous lenses of Zucker diabetic fatty (ZDF) rats, an animal model of type 2diabetes. In cataractous lenses from twenty-oneweek-old ZDF rats, LEC apoptosis was markedly increased,and the accumulation of argpyrimidine as well as subsequent activation of NF-κB in LECs were significantly enhanced. The ratio of Bax to Bcl-2 protein levels was also increased. In addition, the accumulation of argpyrimidine triggered apoptosis in methylglyoxal-treated HLE-B3 cells. However, the presence of pyridoxamine (an AGEs inhibitor) and pyrrolidine dithiocarbamate (a NF-κB inhibitor) prevented apoptosis in HLE-B3 cells through the inhibition of argpyrimidine formation and the blockage of NF-κB nuclear translocalization, respectively. These results suggest that the cellular accumulation of argpyrimidine in LECs is NF-κB-dependent and pro-apoptotic.
-
SOHN, EUNJIN,KIM, JUNGHYUN,KIM, CHAN SIK,JO, KYUHYUNG,KIM, JIN SOOK SPANDIDOS PUBLICATIONS 2015 MOLECULAR MEDICINE REPORTS Vol.12 No.4
<P>Podocyte injury contributes to renal damage and, eventually, to the occurrence of proteinuria in diabetic nephropathy. The aim of the present study was to investigate the effect of an ethanol extract from Rhizoma <I>Polygonum cuspidatum</I> (<I>P. cuspidatum</I>) on proteinuria and podocyte injury, and elucidate the underlying mechanism for streptozotocin (STZ)-induced diabetic nephropathy. The protective effects of <I>P. cuspidatum</I> extract (PCE) on renal podocytes in STZ-induced diabetic rats were also investigated. PCE (100 or 350 mg/kg/day) was administered to STZ-induced diabetic rats for 16 weeks, and blood glucose levels, body weight and proteinuria were measured. A double labeling technique with the terminal deoxynucleotidyl transferase dUTP nick end labeling assay was performed and synaptopodin expression was observed. In addition, cleaved caspase-3, methylglyoxal (MGO) and 8-hydroxydeoxyguanosine (8-OHdG) expression levels were measured. STZ-induced diabetic rats developed hyperglycemia and proteinuria. Increased apoptosis of the podocytes and increased cleaved caspase-3, MGO and 8-OHdG expression levels, as well as decreased synaptopodin expression were detected in the glomeruli of STZ-induced diabetic rats. However, treatment with PCE for 16 weeks restored protein levels to normal, and reduced podocyte loss and apoptosis. Levels of caspase-3 and MGO expression, as well as oxidative stress were ameliorated by PCE treatment. In addition, emodin, a biologically active ingredient of PCE, exerted an MGO scavenging effect and inhibited MGO-derived advanced glycation end-product formation. These findings indicate that PCE may be administered to prevent proteinuria and podocyte loss in STZ-induced diabetic rats partly by inhibiting podocyte apoptosis and cleaved caspase-3 expression, and by restoring the balance of oxidative stress and MGO expression.</P>
-
홍삼가수분해추출물의 db/db 마우스에서 신장 손상 예방효과
김찬식 ( Chan-sik Kim ),조규형 ( Kyuhyung Jo ),표미경 ( Mi Kyung Pyo ),김진숙 ( Jin Sook Kim ),김정현 ( Junghyun Kim ) 대한본초학회 2018 大韓本草學會誌 Vol.33 No.4
Objectives : Diabetic nephropathy is one of the most significant chronic complications of diabetes. Advanced glycation end products (AGEs) have been implicated in the development of diabetic nephropathy. GS-E3D is an enzymatic modified red ginseng extract by pectin lyase and has an increased concentration of the ginsenoside Rd compared to an unmodified red ginseng extract. In this study, we evaluated the preventive effects of GS-E3D on renal dysfunction in the type 2 diabetic db/db mice. Methods : GS-E3D (100 or 250 ㎎/㎏ body weight per day) was given to db/db mice through oral gavage for 6 weeks. Body weight and blood glucose levels were examined. At the end of the experiment, albuminuria was measured. The renal tissues were collected for histological examination, and immunohistochemical staining was used to detect renal accumulation of AGEs and podocyte loss Results : In the db/db mice, severe hyperglycemia developed, and albuminuria was significantly increased. Diabetes induced markedly morphological alterations to the renal glomerular cells. AGE accumulations and podocyte loss were detected in renal glomeruli. No difference in blood glucose levels was noted between GS-E3D-treated and vehicletreated diabetic db/db mice. However, GS-E3D treatment significantly reduced albuminuria and AGE accumulations in diabetic mice. Moreover, the loss of podocytes was restored by GS-E3D treatment. Conclusions : GS-E3D might be beneficial for the treatment of diabetic nephropathy. The ability of GS-E3D on to attenuate albuminuria and podocyte dysfunction in the db/db mice may be mediated by the inhibition of AGE accumulation.
-
The Role of High-Mobility Group Box-1 Protein in the Development of Diabetic Nephropathy
Kim, Junghyun,Sohn, Eunjin,Kim, Chan-Sik,Jo, Kyuhyung,Kim, Jin Sook S. Karger AG 2011 American journal of nephrology Vol.33 No.6
<P>Abstract</P><P><I>Background/Aims:</I> The purpose of the experiment reported here was to assess the involvement of high-mobility group box-1 (HMGB1), receptor for advanced glycation end products (RAGE) and nuclear factor (NF)-κB signaling pathway in the development of rat diabetic nephropathy. <I>Methods:</I> Diabetes was induced by intraperitoneal streptozotocin injection in 7-week-old male rats. At 20 weeks of age, renal expression of HMGB1 was detected by immunohistochemistry. The expression of RAGE and NF-κB activity was studied by Western blot and electrophoretic mobility shift assay in renal tissues of normoglycemic and diabetic rats, respectively. <I>Results:</I> HMGB1 was highly expressed in both the cytoplasmic and nuclear patterns in diabetic renal glomerular cells and tubular epithelial cells, although in normal rats, HMGB1 was expressed only in the cell nuclei. The expression of RAGE, a potential receptor for HMGB1, and NF-κB activity were also greater in diabetic than in normal rats. Moreover, diabetes increased the binding of NF-κB to the RAGE promoter. <I>Conclusion:</I> These findings suggest that hyperglycemia-induced HMGB1 release may induce the renal injury in diabetic rats, and that the pathogenic role of HMGB1 might be dependent on RAGE and through activation of NF-κB.</P><P>Copyright © 2011 S. Karger AG, Basel</P>
ScienceON연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
